The overall aim of the proposed work is to determine whether or not endurance exercise during senescence will reverse the aging-related decline in the cellular properties of the myocardium, thereby leading to an improved myocardial function. Others have suggested that the decreased function of the sarcoplasmic reticulum may be an important factor in the slowing of the isometric contractile duration of cardiac muscle with aging. Moreover, myocardial protein synthesis apparently decreases as the organism ages from maturity to senescence. Therefore, this proposal deals with the examination of the sarcoplasmic reticulum and protein synthesis in greater detail in the hearts of adult and senescent rats followed by the determination of the responsiveness of these two parameters to endurance exercise. The ATP-dependent calcium transport properties of cardiac sarcoplasmic reticulum will be examined using biochemical and morphological techniques to determine (1) calcium flux in relation to the hydrolysis of ATP under a variety of conditions and (2) the density of the calcium transport ATPase, both in situ and in vitro. The rates of myocardial protein synthesis will be estimated for actin, cytochrome c, and ribosomal proteins. The levels of mRNA for both actin and cytochrome c will be measured. Both the sarcoplasmic reticulum and protein synthesis will be examined before and after specified periods of endurance exercise training during senescence. The isometric contractile parameters of isolated papillary muscle will be assessed at each time point of exercise training in order to determine any improvements in myocardial function. These studies will therefore determine the adaptability of cellular factors of the myocardium endurance exercise during senescence in relation to myocardial function. In this manner an insight into those mechanisms involved in the benefitual aspects of exercise during senescence may be gained.